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JAM3 orquesta la fosforilación de AKT dependiente de Mac-1 para facilitar la patogénesis del meningioma impulsada por

Jing Zhang¹, Yipeng Dong¹, Xianghua Zhang¹

¹Department of Neurosurgery, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China.

Cellular signalling

|January 7, 2026

Abstract:

Despite the documented involvement of neutrophil extracellular traps (NETs) in various cancer types, their specific role in meningioma development remains understudied. Here, we report a mechanism by which the JAM3/Mac-1 interaction promotes meningioma development via NETs. We found that JAM3 knockdown in meningioma cells suppressed AKT phosphorylation, thereby reducing neutrophil migration and NET formation in co-culture; these effects were rescued by the AKT activator SC79. Co-IP confirmed the JAM3/Mac-1 interaction. In a xenograft model, JAM3 knockdown inhibited tumor growth and intratumoral NETs. Furthermore, NETs enhanced meningioma cell growth in vitro and in vivo, an effect abolished by DNase I. Conversely, Mac-1 knockdown in neutrophils impaired their function, which was also restored by SC79. Clinically, JAM3 expression correlated with Mac-1 and NET markers in meningioma samples. In conclusion, JAM3 promotes meningioma development by regulating the formation of NET through the Mac-1/AKT axis. These findings offer novel insights for treating these common primary tumors of the central nervous system.

Palabras clave:

AKT JAM3 Mac-1 Meningioma Neutrófilo Trampas extracelulares de neutrófilos (NET)

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